Cardioprotective effect against ischemia-reperfusion injury of AHC-52, a dihydropyridine compound with inhibitory effect on Cl- but not Ca2+ current.
We examined the effects of a dihydropyridine compound, AHC-52, on guinea pig myocardium. In ventricular cardiomyocytes, AHC-52 (1 microM) had no effect on the basal peak inward and steady state currents, but inhibited the isoprenaline-induced time independent Cl- current. In coronary perfused right ventricular preparations, no-flow ischemia induced decreases in developed tension which recovered only to about 50% of initial values after reperfusion. AHC-52 (0.1 microM) had no effect on developed tension under normal conditions and during ischemia, but significantly improved the recovery of developed tension after reperfusion to about 80% of preischemic values. Thus, AHC-52 inhibits Cl- channels in cardiac muscle and may have protective effects against ischemia-reperfusion injury.
Tanaka
H
H
Department of Pharmacology, Toho University School of Pharmaceutical Sciences, Chiba, Japan.
Sekine
T
T
Terada
M
M
Kobayashi
Y
Y
Shigenobu
K
K
D000818:Animals; D015220:Calcium Channels / Q000187:drug effects*; D002478:Cells, Cultured; D018118:Chloride Channels / Q000187:drug effects*; D004095:Dihydropyridines / Q000494:pharmacology*; D006168:Guinea Pigs; D006321:Heart / Q000187:drug effects*; D006352:Heart Ventricles / Q000187:drug effects; D066298:In Vitro Techniques; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control; D009206:Myocardium / Q000378:metabolism; D018408:Patch-Clamp Techniques; D011720:Pyrazoles / Q000494:pharmacology*; D016276:Ventricular Function
D015220:Calcium Channels; D018118:Chloride Channels; D004095:Dihydropyridines; D011720:Pyrazoles; C059017:AHC 52